Cardiovascular disease 1 Flashcards
1
Q
Define ischaemic heart disease
A
- Inadequate blood supply to the myocardium due to
1) reduced coronary blood flow-atheroma/thrombus
2) myocardial hypertrophy usually due to systemic hypertension
2
Q
What is the pathogenesis of IHD?
A
- Acute & chronic ischaemia
- Autorgulation of coronary blood flow breaks down in occlusion
- Low diastolic flow esp in subendocardial tissue
- Active aerobic metabolism of cardiac muscle
- Myocyte dysfunction/death due to ischaemia
3
Q
Name some IHD syndromes and risk factors
A
- Angina Pectoris: stable, unstable, variant
- Acute coronary syndrome: acute MI, unstable angina
- Sudden cardiac death
- Chronic IHD
- Smoking, obesity, high cholesterol, hypertension,diabetes
4
Q
Describe acute ischaemia
A
- Atheroma & acute thrombosis/haemorrhage
- Lipid rich plaques most unstable
- Regional transmural MI
- Treatment-thrombolysis
- Causes myocardial stunning
- Diagnosis-clinical, blood cardia proteins
5
Q
Describe an MI morphology
A
- 1 week= pale, thin, granulaton tissue & fibrosis
- After 4 weeks dense fibrous scar cannot tell how old MI is
6
Q
Describe a subendocardial MI, how is this different to transmural MI?
A
- Subendocardial myocardium poorly perfused
- Subendocardial myocardium can infarct without any acute coronary occlusion
- SMI= area of ischemic necrosis is limited to the endocardium
- TMI= Ischaemic necrosis of full thickness of myocardium
7
Q
What blood markers are used to check cardiac myocyte damage?
A
- Troponin I & T= detectable upto 7days after, raised post MI & pulmonary embolism, HF, myocarditis
- Creatine Kinase= detectable upto 3 days after
8
Q
What are complications of an MI?
A
- Arrhythmia=VF& sudden death
- Ischaemic pain
- Left V failure & shock
- Pericarditis
- Cardiac mural thrombus & emboli
- DVT &PE
- Myocardial rupture-tamponade, V septal perforation, papillary muscle rupture
- Ventricular aneurysm
- Autoimmune pericarditis
9
Q
Describe chronic IHD
A
- Coronary artery atheroma produces myocardial ischaemia & angina on exertion
- Risk of sudden death/MI
- Unstable angina evolving
- Variant angina- coronary arterial spasm
10
Q
What is familial hypercholestrolaemia?
A
- Mutation in genes involved in cholesterol metabolism: Apolipoprotein B, Low density lipoprotein receptor gene
- Autosomal dominant
- Heterozygous-develop xanthomas, corneal Marcus, early atherosclerosis treat with statins
11
Q
What are causes of primary hypertension?
A
- Physiological systems interacting over long periods of time
- Cardiac baroreceptors
- Renin-angiotensin-aldosterone system
- Kinin-kallikrekin system
- Naturetic peptides
- Autonomic NS
- Adrenergic receptor system
- Autocrine factors produced by blood vessels
12
Q
How can sodium cause hypertension?
A
- All inherited forms share inc net salt balance as common pathway
- Inc intravascular vol & vol delivery to heart augment CO & BP
- Resulting tissue perfusion exceeds metabolic demand leading to auto regulation of blood flow to inc vasoC to reduce blood flow
- Results in steady state hemodynamic pattern of elevated BP w/inc systemic vascular resistance & normal CO
13
Q
Name the main causes of secondary hypertension
A
- Renal: renal stenosis
- Endocrine: hyperthyroidism
- Cardiovascular
- Neurologic
- Phaeochromocytoma
14
Q
Describe the Renin-Angiotensin-Aldosterone pathway
A
- Renin= synthesised, stored &released from juxtaglomerular apparatus in wall of afferent arterioles of kidney. Cleaves angiotensinogen to angiotensin I
- Angiotensin I–>angiotensin II (active)
- Angiotensin II=potent vasoC, short 1/2 life, stimulates adrenal cortex to produce aldosterone
- Aldosterone= mineralocorticoid, renal action causes Na & H2O retention, circulating blood vol inc
15
Q
What is renal artery stenosis and how can this lead to hypertension?
A
- Reduced BP in kidney- afferent arterioles
- Juxtaglomerular apparatus stimulated to produce renin
- Renin-angiotensin system stimulates adrenal cortex zona glomerulosa cells to produce aldosterone= inc BP
